Neurotoxicity of amyloid β-protein: synaptic and network dysfunction.
By L. Mucke, D. Selkoe. Cold Spring Harbor Perspectives in Medicine, 2012
985 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Pharmacology, Physiology
View Paper: https://www.semanticscholar.org/paper/83dd801362bfea8a89d8ab28f22eb52ef07e5c5e
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cellular and Molecular Neuroscience
- Nora D. Volkow
- Gene-Jack Wang
- Dardo Tomasi
- B. Barres
- Beth Stevens
- D. Selkoe
- G. Koob
- Kent C. Berridge
In Pharmacology
In Physiology
Citations in the corpus
- Spatial Transcriptomics and In Situ Sequencing to Study Alzheimer's Disease. (2020, background): “We leave open the discussion of what form of Ab might trigger the pathological changes; some groups have suggested that a toxic halo of oligomeric Ab surrounding amyloid plaques is the bioactive agent (Koffie et al., 2009; Mucke and Selkoe, 2012).”
- β-Amyloid accumulation in the human brain after one night of sleep deprivation (2018, background): “Notably, increased ABB in the brain has been associated with impairment of brain function (11, 12).”
- Complement and Microglia Mediate Early Synapse Loss in Alzheimer Mouse Models (2016, positive): “Alternatively, oAβ binding to synapses may weaken the synapse (4) and expose a C1q receptor.”